Dr. Kerschner added, “We are also working in our lab on a more direct approach—that is, treatments that actually do counteract pepsin activation. But we’re quite a ways off from bringing that to fruition.”
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December 2013Nancy Bauman, MD, a pediatric otolaryngologist at Children’s National Medical Center in Washington, DC, and an ENTtoday editorial board member, noted that regardless of where pepsin originates, “once it gets into the upper airway, the enzyme can do considerable damage.” Thus, the paper by Kerschner and colleagues “really has the potential to be seminal; this could bring about a significant change in how we view the role of extraesophageal reflux in chronic lung disease, how we diagnose the condition and, hopefully, how we treat it.”
Dr. Bauman still wonders if it is possible that the pepsin detected in this study could have come from a source other than the stomach. “We assume that pepsin arises only in the stomach, but I am not sure that we can exclude the possibility of airway epithelial metaplasia as a source of pepsin production. I also understand that some species of Aspergillus produce pepsin-like proteases but I assume that there would not be enough homology between such fungal proteases and human pepsin to be detected by the pepsin assay used in this study. Regardless of the source of pepsin, targeting inactivation of it will be the key to successfully treating these patients and the work of Dr. Kerschner and Dr. Nikki Johnston’s lab is very exciting.”—DB